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Year : 2005  |  Volume : 53  |  Issue : 2  |  Page : 241-242

Authors' Reply

1 Departments of Neurology, The Institute of Neurological Sciences, CARE Hospital, Hyderabad, India
2 Nizam’s Institute of Medical Sciences, Hyderabad, India

Date of Acceptance23-May-2005

Correspondence Address:
J M K Murthy
Departments of Neurology, The Institute of Neurological Sciences, CARE Hospital, Hyderabad
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Source of Support: None, Conflict of Interest: None

PMID: 16010072

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How to cite this article:
Murthy J M, Meena A K, Chowdary G V, Narayanan T J. Authors' Reply. Neurol India 2005;53:241-2

How to cite this URL:
Murthy J M, Meena A K, Chowdary G V, Narayanan T J. Authors' Reply. Neurol India [serial online] 2005 [cited 2020 Jan 18];53:241-2. Available from:


We thank Kumar and colleagues for his interest in our article published in the March issue of the journal.[1] All the patients were established cases of myasthenia gravis (MG) under follow up in our clinic. The initial diagnosis in the patients was established by neostigmine test and decrement response. This has been stated in the material and methods. We had not used neostigmine to establish the diagnosis of myasthenic crisis in our series. We are very much aware of the safety and superiority of edrophonium over neostigmine, unfortunately the availability is a major limiting factor. A cholinergic crisis is less common than presumed and combination of both crises is often clinically encountered as seen in one of the patients in our series.[2]

Steroids were started in all the patients after disease stabilization while they were in the hospital. The initiation to steroids was gradual. Worsening with high-dose steroid occurs 7-14 days after initiation of the high doses and usually lasts less than 1 week. It appears that gradually increasing the dose of steroids over a period reduces the risk of the early worsening of the disease.[3]

In patients with MG uncontrolled studies, plasma exchange (PE) have demonstrated efficacy with the onset of improvement within the first week.[4],[5] Randomized controlled studies comparing PE with intravenous immunoglobulin (IVIg) have demonstrated equal efficacy, but significantly fewer and less severe side effects for the IVIg.[6],[7] The data on the efficacy of both these immunomodulators in myasthenic crisis are limited. In a retrospective multicenter study PE (compared with IVIg) was associated with a superior ventilatory status at 2-week and 1-month functional outcome. However, the complication rate was higher with PE compared with IVIg.[8]

 » References Top

1.Murthy JMK, Meena AK, Chowdary GVS, Narayanan TJ. Myasthenic crisis: Clinical features, complications and mortality. Neurol India 2005: 53: 37-40.  Back to cited text no. 1    
2.Thomas CE, Mayer SA, Gungor Y, Swarup R, Webster EA, Chang I, et al . Myasthenic crisis: Clinical features, mortality complications and risk factors for prolonged intubation. Neurology 1997; 48: 1253-60.  Back to cited text no. 2    
3.Seybold ME, Drachman DB. Gradually increasing doses of prednisone in myasthenia gravis. Reducing the hazards of treatment. N Engl J Med 1974; 290: 81-4.   Back to cited text no. 3    
4.Pinching AJ, Peters DK. Remission of myasthenia gravis following plasma exchange. Lancet 1976; 2: 1373-6.  Back to cited text no. 4    
5.Dau PC, Lindstrom JM, Cassel CK, Denys EH, Shev EE, Spitler LE. Plasmapheresis and immunosuppressive drug therapy in myasthenia gravis. N Engl J Med 1977; 297: 1134-40.  Back to cited text no. 5    
6.Gajdos P, Chevert S, Clair B, Tranchant C, Chastang C. Clinical trial of plasma exchange and high-dose intravenous immunoglobulin in myasthenia gravis. Myasthenia Gravis Clinical Study. Ann Neurol 1997; 41: 789-96.  Back to cited text no. 6    
7.Ronager J, Ravnborg M, Hermansen I, Vorstrup S. Immunoglobulin treatment versus plasma exchange in patients with chronic moderate to severe myasthenia gravis. Artif Organs 2001; 25:96773.   Back to cited text no. 7    
8.Qureshi AI, Choudary MA, Akbar MS, et al . Plasma exchange versus intravenous immunoglobulin treatment in myasthenic crisis. Neruology 1999; 52: 629-32.   Back to cited text no. 8    

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